Venom from the ectoparasitoid wasp Eulophus pennicornis disrupts host ecdysteroid production by regulating host prothoracic gland activity

Attack by the ectoparasitoid Eulophus pennicornis Nees (Hymenoptera: Euloph idae) prevents larvae of Lacanobia oleracea L. (Lepidoptera: Noctuidae) fro m moulting. Prothoracic glands (PGs) excised from parasitized or artificial ly envenomated hosts show a reduced basal level of ecdysteroid release at a time when non-parasitized caterpillars produce an ecdysteroid surge (48 h post moult to 5th stadium = penultimate stadium in non-venomated hosts). By contrast, PGs from similarly parasitized or envenomated caterpillars relea se comparatively high levels of ecdysteroid at 120 h post-moult. Temporary inactivation of PGs cannot be attributed solely to a parasitoid-induced red uction in cell viability, and incubation in E. pennicornis venom in vitro d oes not exert any direct effect on either PG cell viability or ecdysteroid release. However, inactivated PGs are not stimulated by forskolin, which ma y indicate that, the absence of the required pre-moult ecdysteroid surge in developmentally arrested L. oleracea is due to insensitivity to a prothora cicotropic hormone. Even though parasitized caterpillars never moult, rever sed-phase HPLC separations and radioimmunoassay confirm that they produce a ctive moulting hormone (20-hydroxyecdysone) at 120 h post-moult. These resu lts suggest that E. pennicornis arrests host development through the indire ct effects on their hosts' PGs. This effect is not achieved through the des truction of gland cells, but more likely reflects the interruption of an in nate cycle in PG activity, such that they lose their ability to respond to a normal cue to produce an essential hormone peak at a crucial point in dev elopment.